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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The syndrome of immediate type I food hypersensitivity, mediated by tissue-bound IgE antibody and mast cell histamine release, is well recorded in the medical literature. This case study represents a previously undescribed late food hypersensitivity, induced only by strenuous exercise. Identification of this new syndrome illustrates classical epidemiologic analysis, improves medical advice for the allergic and athletically inclined, and raises new questions in the areas of allergy and immunology.
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PMID:Exercise-induced anaphylactic reaction to shellfish. 44 45

The clinical course of twenty-one patients who presented with life-threatening symptoms, appearing to be allergic in aetiology, is described. In ten of these patients clinical evaluation established a diagnosis, for example: drug allergy, food allergy, a curious form of hospital addiction syndrome, an underlying malignancy, systemic mast cell disease or a complement abnormality. In the remaining subjects, it was found that their condition could be stabilized with sympathomimetics, antihistamines and corticosteroids. In those in whom no aetiology could be found, there was usually a spontaneous subsidence of the frequency and severity of attacks or spontaneous remission. No fatalities occurred.
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PMID:Evaluation of severe (anaphylactic) reactions. 66 3

Food hypersensitivity is reported to play an immunopathogenic role in atopic dermatitis in approximately one-third of children. In 320 selected children with moderate to severe atopic dermatitis, 63% of children were found to have food hypersensitivity by double-blind placebo-controlled food challenges. Both IgE-mediated mast cell and mononuclear cell activation appear responsible for the eczematous lesions resulting from ingestion of food allergens.
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PMID:The immunopathogenic role of food hypersensitivity in atopic dermatitis. 147 32

Mast cells are a significant component of the mucosa in the gastrointestinal tract. There is increasing evidence that these cells are involved in the pathophysiology of various intestinal disorders ranging from food allergy to inflammatory bowel disease. When activated, mast cells release a host of potent mediators and cytokines which are capable of inducing pathophysiology. The bulk of the evidence has come from hypersensitivity studies in experimental animals sensitized either by parasitic infection or by active immunization to an antigen using adjuvants which stimulate IgE production. Subsequent antigen challenge of the gut results in mast cell activation associated with alterations in intestinal functions including ion transport and epithelial permeability. Intestinal secretory transport responses are inhibited by antagonists of mast cell mediators and neurotoxins, implicating mast cell-nerve interactions with the epithelium. In genetically mast cell-deficient mice, antigen-induced secretion is reduced approximately 70% and this component is not affected by neural or mast cell inhibitors; adoptive transfer of bone marrow containing mast cell precursors derived from congenic normal mice restores the complete antigen response. These results provide more direct proof that mast cell activation causes abnormal gut function. Recently, we have begun studies which indicate that activation of mast cells induces ion secretion in surgically resected human intestine. Reduced secretory responses in specimens from patients with IBD suggest that mast cells may play a role in the pathophysiology of inflammatory bowel disease.
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PMID:Functional abnormalities in the intestine associated with mucosal mast cell activation. 150 88

Food allergy (FA) is a very important problem affecting numbers of infants and children with protean manifestations which are frequent challenges to the pediatrician and other specialists working with children. Adverse reactions to food are very complex, frequently mediated bu IgE mechanisms, and often by other mechanisms. To make the correct diagnosis and to arrive at a proper therapeutic approach requires all the skill a physician can gather. Only an extensive knowledge of the various mechanisms and pharmacologic agents that can be used to prevent or treat these adverse reactions will allow the physician to approach the problem scientifically and come to a reasonable solution for the patient. The role of dietary factors in atopic dermatitis (AD) has long been a subject of controversies. However, it has been shown that FA plays a role in some children with AD. Therefore, the management of this multifaceted disorder is a challenge for pediatricians, dermatologists, and allergists. SCG, which is the salt of a bis-chromone carboxylic acid, has been shown to be of proven efficacy in the prophylaxis of bronchial asthma, allergic rhinitis, and of other disorders associated with mast cell degranulation. The drug has different modes of action, such as inhibition of rat passive cutaneous anaphylaxis, and the antigen-induced histamine release from passively sensitized peritoneal cells. Recently, clinical studies indicated that SCG has a direct effect on inflammatory cells, inhibiting either various leukocyte functions (membrane receptor expression, cytotoxic capacity), or "in vitro" activation of human neutrophils, eosinophils and monocytes. Although SCG has been widely used for the management of respiratory allergy, conflicting results of FA treatment have been reported by several authors. We have reviewed 18 papers on the use of SCG in the management of children with FA, which included 341 children aged 0.5-15 years. In this paper we discuss 12 studies reporting 281 children affected with AD.
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PMID:Food allergy in children: diagnosis and treatment with sodium cromoglycate. 170 97

The in vitro histamine release response of human intestinal mast cells and basophils challenged with anti-IgE, Concanavalin A, ionophore A23187 and food extracts was compared with skin prick test, RAST analysis and open food challenge. It was not possible to perform food challenge in all patients; however, seven children underwent open food challenge and in five the clinical diagnosis of "true" food allergy was confirmed. The intestinal mast cells were pooled from enzymatically dispersed duodenal biopsies obtained by duodenoscopy from 15 selected children suspected of food allergy, and five age-matched controls. In nine of 10 patients classified as "food allergic" intestinal mast cells released histamine to various food extracts in a dose-dependent fashion. From the mast cells of the nine food-allergic patients compared with non-allergics, the anti-IgE mediated mast cell histamine release was increased. Additionally, at 1000 U/ml anti-IgE the mast cell histamine release was increased compared with their corresponding basophils. However, in non-allergic subjects the histamine release of basophils was increased compared with their corresponding mast cells. Histamine release from basophils was positively correlated to the test scores of the RAST analysis, skin prick test, and food challenge. No apparent correlation between tests scores obtained from histamine release of intestinal mast cell and the other tests was demonstrated, except in children with diarrhoea as only symptom. However, the study gives evidence that duodenal mast cells actually are sensitized with specific IgE and thus may play a pathophysiological role in food hypersensitivity. In addition, the study shows that the ability of different stimuli, including food extracts, to trigger basophil histamine release does not correlate with their potency to induce histamine release from mast cells.
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PMID:Comparison of intestinal mast cell and basophil histamine release in children with food allergic reactions. 248 85

Nine biopsy specimens from the jejunum of patients with a clinical history of food allergy and 10 from the rectal mucosa of patients with presumed 'allergic proctitis' were fixed in cold ethanol and further processed for paraffin embedding. Serial tissue sections were stained for IgE by direct (polyclonal antibody) and indirect (monoclonal antibody) immunofluorescence methods. Adjacent sections were subjected to conventional mast cell staining (astra blue). In all mucosal specimens from the jejunum and in 8 rectal ones, numerous cells were found to be positive both for astra blue by transmission microscopy and for IgE by fluorescence microscopy of the same section. With the monoclonal antibody all astra-blue-positive cells were IgE-positive; however, this was not always the case with the polyclonal reagent, probably because the fluorescence was weaker with the direct technique. Detection of IgE-positive mucosal mast cells may turn out to be of diagnostic interest in patients with adverse reactions to food.
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PMID:IgE-positive cells in human intestinal mucosa are mainly mast cells. 266 1

The aim of our study was to determine whether patients suffering from food allergy show any pathologic reactions on the mucosa of the gastrointestinal (GI) tract after allergen contact. For this reason, we included in the study 30 patients whose food-allergic history had been proven through double-blind challenge tests; 20 healthy volunteers also were included as controls. The patients and volunteers underwent standard laboratory investigations and allergy tests with PRICK and RAST. To observe possible mucosal reactions, we applied the proposed allergens via endoscope to the gastric mucosa. Macroscopic reactions were observed blindly by two independent physicians. Biopsies were taken from the challenged areas for histological and histochemical analysis. The examinations included the estimations of tissue histamine concentrations and of mast cell and lymphocyte counts. In all 30 patients, macroscopic reactions (swelling, erosions, bleedings) were observed. Patients with food allergy had, in contrast to healthy volunteers, elevated lymphocyte counts, tissue histamine concentrations, and mast cell counts. After provocation, tissue histamine concentrations and mast cell counts fell significantly. Skin and RAST tests showed positive results in only 46.7% and 50.0%, respectively, of food-allergic patients. We conclude, first, that through intragastric provocation under endoscopic control (IPEC), food-allergic reactions on the mucosa of the GI tract can be verified and, second, that the liberation of tissue histamine seems to play an important role in the establishment of food-allergic reactions on the mucosa.
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PMID:Gastric mucosal reactions in patients with food allergy. 318 62

The role of IgE-mediated hypersensitivity in the development of middle ear disease has not been completely resolved. However, on the basis of our investigations and those of other laboratories, we suggest that approximately two thirds of patients with chronic recurrent otitis media do not have allergies. The other third may have allergic rhinitis, and this allergic rhinitis could play a direct role in producing eustachian tube dysfunction in recurrent otitis media. However, viral infections of the upper respiratory tract may also induce IgE-mediated release of mast cell inflammatory mediators, and could cause otitis media on the basis of viral infection alone. Subtle immunologic deficiencies involving the IgG2 subclass and other immunoglobulin subclasses may also be lower in otitis-prone children, and this may be a genetically inherited disorder. Finally, the possibility of food allergy in otitis media must be considered, particularly in the young otitis-prone child with chronic recurrent otitis media.
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PMID:Recent advances in immunologic reactivity in otitis media with effusion. 328 24

In fourteen patients with food allergy, intragastral provocation under endoscopical control (IPEC) was performed. In all patients positive immediate-type reactions of the gastric mucosa were observed consisting of oedema, erythema and petechial bleeding. Microscopically, mast cell degranulation was observed and measured by mast cell counts using the o-phthaldialdehyde technique. Concomitantly, tissue histamine content in gastric mucosa decreased significantly after allergen provocation, while there was no change in normal volunteers. Plasma histamine concentration increased in most patients; the increases were most evident in four patients showing mild systemic reactions (urticaria and bronchospasm). The technique described might prove to be useful in establishing the diagnosis in doubtful cases of food allergy.
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PMID:Intragastral provocation under endoscopic control (IPEC) in food allergy: mast cell and histamine changes in gastric mucosa. 399 25


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